1996 Fiscal Year Final Research Report Summary
The Effect of Neurotrophic Factor MK on the Expression and Repair of Brain injury
| Project/Area Number |
07670718
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Neurology
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| Research Institution | Kagoshima University |
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Principal Investigator |
YOSHIDA Yoshihiro School of Allied Medical Sciences, Kagoshima University Assistant Professor, 医療技術短期大学部, 助教授 (10107906)
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| Co-Investigator(Kenkyū-buntansha) |
OZAWA Masayuki Faculty of Medicine, Kagoshima University Professor, 医学部, 教授 (90136854)
OSAME Mitsuhiro Faculty of Medicine, Kagoshima University Professor, 医学部, 教授 (10041435)
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| Project Period (FY) |
1995 – 1996
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| Keywords | Neurotrophic factor / Midkine / cerebral infarction / rat / GFAP / astrocytes |
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| Research Abstract |
Midkine (MK) was found as a product of retinoic acid responsive gene and a protein, which has a promoting effect of growth or diferetiation on the cultured cells. It is so called on of the neurotrophic factor because of the repairing effects of the degeneration of neuron in culture. We found that MK express penubral area around the infarct of rat experimental infarct in the early stage. Furthermore, MK were found in the astrocytic cytoplasm in 2 days after the infarction by double staining of both anti-glial fibrillary acidic protein antibody and anti-MK antibody. MK was found in the neuropil on the 4 days after the infarction, where MK was stained in the swollen astrocytic processes. AP-1 responsive element was recognized in the upper sites of MK genom. Accordingly MK was thought to express through the AP-l, immediate early gene product. In human cerebral infarctin MK was expressed in the early stage.
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